The role of platelet hyperfunction in thrombus formation in hyperlipidemia.
The mechanism of thrombus formation in hyperlipidemia was studied. Attempts at artificial creation of an arterial thrombus in control rabbits stenosing the femoral artery by ligature were not successful unless ellagic acid was administered by injection. However, in rabbits with hyperlipidemia, mere creation of stenosis in the femoral artery resulted in a high percentage of thrombus formation. In rabbits with hyperlipidemia, both thromboxane (Tx) A2 biosynthesis in platelets and prostacyclin (PGI2) biosynthesis in the aorta were increased and these changes were noted at the level of cyclooxygenase in the arachidonic acid metabolic pathway. Therefore, these results suggest that thrombi are likely to be formed in hyperlipidemia and that such thrombus formation is due largely to platelet hyperfunction.
D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D001777:Blood Coagulation; D001792:Blood Platelets / Q000378:metabolism*; D005263:Femoral Artery / Q000503:physiopathology; D006949:Hyperlipidemias / Q000097:blood* / Q000150:complications; D008297:Male; D010314:Partial Thromboplastin Time; D010974:Platelet Aggregation; D011460:Prostaglandins F / Q000096:biosynthesis; D011463:Prostaglandins H / Q000378:metabolism; D011517:Prothrombin Time; D011817:Rabbits; D013927:Thrombosis / Q000150:complications; D013929:Thromboxane B2 / Q000096:biosynthesis
D001095:Arachidonic Acids; D011460:Prostaglandins F; D011463:Prostaglandins H; D016718:Arachidonic Acid; D013929:Thromboxane B2; C100006:prostaglandin F1